Contributions
Abstract: EP1535
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: In multiple sclerosis (MS), FLAIR or T2 magnetic resonance images (MRI) are used to identify new white matter hyperintensities (WMH) as an important measure of treatment efficacy. However, WMH detected with these techniques are pathologically non-specific and can appear independent of demyelinating processes due to hypertension or aging. Quantitative MRI may help to differentiate lesions that look identical on FLAIR but differ pathologically.
Goal: To investigate the magnetic susceptibility (QSM) and R2* of WMH in relapsing-remitting MS, clinically isolated syndrome (CIS), concussion (CC) and dementia (DEM).
Methods: 3T QSM MRI data, together with FLAIR or T2, were acquired in 3 patients each of the 4 cohorts. QSM and R2* were estimated from the phase and magnitude of multi-echo gradient scans. After Laplacian unwrapping and V-SHARP, QSM maps were created using in-house software. R2* maps were obtained by linear fitting to the logarithmic data. WMH were manually defined on registered FLAIR or T2 scans. To establish the lesion contrast (iso/hypo/hyper-intensity), peri-lesional WM masks were defined by mask-dilation and subtraction of the original mask. Average ΔQSM-χ and ΔR2* values for each WMH were assessed.
Results: 19/43/30 and 38 lesions were identified in CC, DEM, CIS and MS(median age=20/82/19/62yrs). QSM-hypointensities were present across disorders, with increasing hypointensity, reflective of iron loss, in CIS and MS lesions (ΔχCC=-5.3/ΔχMS=-18.7ppb).
CC-WMH presented as predominantly QSM-isointense (57.9%,Δχ=-0.3ppb), in agreement with an inflammatory response, compared to DEM-WMH, which appeared equally iso- and hyperintense
(39.5% both,Δχ=0.6/9.7ppb) in response to a dilation of perivascular spaces and the development of mild myelin pallor (Udaka 2002,Ann NY Acad Sci).
R2*-hypointensities dominated DEM and MS (79%/84.2%,ΔR2*=-4.6/-6.8Hz), confirming that MS lesions largely represent myelin and iron loss.
In contrast, iso- and hypointense WMH were similarly found in CC and CIS (42%/52%,ΔR2*=-1.9/-3.7Hz; 48/51%,ΔR2*=-0.5/-4.6Hz), suggestive of lesser damage and possibly greater capability to repair in these younger cohorts.
The majority of CIS and MS lesions was QSM-hyperintense (55% both,Δχ=14.2/21.3ppb), in line with the presence of edema, axonal and myelin damage (Li 2016,JMRI).
Conclusion: With its sensitivity to microstructure, QSM differentiates MS lesions from other FLAIR-WMH, while the complementary, less-specific R2* is reduced in most WMH.
Disclosure: Data acquisition was funded by the MS Society of Canada and the Alzheimer Society of Canada.
Vanessa Wiggermann is supported by a Graduate Student Award from the MS Society of Canada.
Christian Kames has nothing to disclose.
GY Robin Hsiung received funds as a site investigator for clinical trials sponsored by TauRx, Roche, EliLilly, AstraZeneca, Biogen, Merck, and Genentech; participated in educational program development sponsored by Merck and research support from CIHR and the Alzheimers Society of BC.
Luanne Metz received grant support from Hoffman La Roche.
David Li has received research funding from the Canadian Institute of Health Research and Multiple Sclerosis Society of Canada. He is the Emeritus Director of the UBC MS/MRI Research Group which has been contracted to perform central analysis of MRI scans for therapeutic trials with Novartis, Perceptives, Roche and Sanofi-Aventis. The UBC MS/MRI Research Group has also received grant support for investigator-initiated independent studies from Genzyme, Merck-Serono, Novartis and Roche. He has acted as a consultant to Vertex Pharmaceuticals and served on the Data and Safety Advisory Board for Opexa Therapeutics and Scientific Advisory Boards for Adelphi Group, Celgene, Novartis and Roche. He has also given lectures which have been supported by non-restricted education grants from Teva, Novartis and Biogen.
Anthony Traboulsee receives research support from Biogen, Chugai, CIHR, Roche, Michael Smith Foundation and the MS Society of Canada; and acts as consultant for Biogen, Roche, EMD Serono, Teva Pharmaceuticals.
Alexander Rauscher receives research support from the Natural Sciences and Engineering Research Council of Canada and the National MS Society.
Abstract: EP1535
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: In multiple sclerosis (MS), FLAIR or T2 magnetic resonance images (MRI) are used to identify new white matter hyperintensities (WMH) as an important measure of treatment efficacy. However, WMH detected with these techniques are pathologically non-specific and can appear independent of demyelinating processes due to hypertension or aging. Quantitative MRI may help to differentiate lesions that look identical on FLAIR but differ pathologically.
Goal: To investigate the magnetic susceptibility (QSM) and R2* of WMH in relapsing-remitting MS, clinically isolated syndrome (CIS), concussion (CC) and dementia (DEM).
Methods: 3T QSM MRI data, together with FLAIR or T2, were acquired in 3 patients each of the 4 cohorts. QSM and R2* were estimated from the phase and magnitude of multi-echo gradient scans. After Laplacian unwrapping and V-SHARP, QSM maps were created using in-house software. R2* maps were obtained by linear fitting to the logarithmic data. WMH were manually defined on registered FLAIR or T2 scans. To establish the lesion contrast (iso/hypo/hyper-intensity), peri-lesional WM masks were defined by mask-dilation and subtraction of the original mask. Average ΔQSM-χ and ΔR2* values for each WMH were assessed.
Results: 19/43/30 and 38 lesions were identified in CC, DEM, CIS and MS(median age=20/82/19/62yrs). QSM-hypointensities were present across disorders, with increasing hypointensity, reflective of iron loss, in CIS and MS lesions (ΔχCC=-5.3/ΔχMS=-18.7ppb).
CC-WMH presented as predominantly QSM-isointense (57.9%,Δχ=-0.3ppb), in agreement with an inflammatory response, compared to DEM-WMH, which appeared equally iso- and hyperintense
(39.5% both,Δχ=0.6/9.7ppb) in response to a dilation of perivascular spaces and the development of mild myelin pallor (Udaka 2002,Ann NY Acad Sci).
R2*-hypointensities dominated DEM and MS (79%/84.2%,ΔR2*=-4.6/-6.8Hz), confirming that MS lesions largely represent myelin and iron loss.
In contrast, iso- and hypointense WMH were similarly found in CC and CIS (42%/52%,ΔR2*=-1.9/-3.7Hz; 48/51%,ΔR2*=-0.5/-4.6Hz), suggestive of lesser damage and possibly greater capability to repair in these younger cohorts.
The majority of CIS and MS lesions was QSM-hyperintense (55% both,Δχ=14.2/21.3ppb), in line with the presence of edema, axonal and myelin damage (Li 2016,JMRI).
Conclusion: With its sensitivity to microstructure, QSM differentiates MS lesions from other FLAIR-WMH, while the complementary, less-specific R2* is reduced in most WMH.
Disclosure: Data acquisition was funded by the MS Society of Canada and the Alzheimer Society of Canada.
Vanessa Wiggermann is supported by a Graduate Student Award from the MS Society of Canada.
Christian Kames has nothing to disclose.
GY Robin Hsiung received funds as a site investigator for clinical trials sponsored by TauRx, Roche, EliLilly, AstraZeneca, Biogen, Merck, and Genentech; participated in educational program development sponsored by Merck and research support from CIHR and the Alzheimers Society of BC.
Luanne Metz received grant support from Hoffman La Roche.
David Li has received research funding from the Canadian Institute of Health Research and Multiple Sclerosis Society of Canada. He is the Emeritus Director of the UBC MS/MRI Research Group which has been contracted to perform central analysis of MRI scans for therapeutic trials with Novartis, Perceptives, Roche and Sanofi-Aventis. The UBC MS/MRI Research Group has also received grant support for investigator-initiated independent studies from Genzyme, Merck-Serono, Novartis and Roche. He has acted as a consultant to Vertex Pharmaceuticals and served on the Data and Safety Advisory Board for Opexa Therapeutics and Scientific Advisory Boards for Adelphi Group, Celgene, Novartis and Roche. He has also given lectures which have been supported by non-restricted education grants from Teva, Novartis and Biogen.
Anthony Traboulsee receives research support from Biogen, Chugai, CIHR, Roche, Michael Smith Foundation and the MS Society of Canada; and acts as consultant for Biogen, Roche, EMD Serono, Teva Pharmaceuticals.
Alexander Rauscher receives research support from the Natural Sciences and Engineering Research Council of Canada and the National MS Society.